Category Archives: Neuroscience

Neuroscience

Empyrean Neuroscience Launches with $22M Series A and Genetic Engineering Platform to Advance Pipeline of Neuroactive Compounds Targeting CNS…

NEW YORK & CAMBRIDGE, England--(BUSINESS WIRE)--Empyrean Neuroscience, Inc., a leading genetic engineering company dedicated to developing neuroactive compounds to treat neuropsychiatric and neurologic disorders, today announced that it has launched with a $22 million Series A financing and a genetic engineering platform to advance a pipeline of neuroactive compounds targeting disorders of the central nervous system (CNS). The company is founded on a proprietary platform designed to genetically engineer small molecule therapeutics from fungi and plants. Veteran biotech executives Usman Oz Azam, M.D., Chief Executive Officer, and Fred Grossman, D.O., FAPA, Chief Medical Officer, lead the company.

Through precision targeting and engineering of the fungal and plant genomes, Empyrean is working to enhance and modulate neuroactive compounds produced by these kingdoms. The platform is being used to identify therapeutic fungal alkaloids, cannabinoids, and other small molecules that may exhibit enhanced efficacy and safety. In addition, the platform is designed to discover novel small molecules that may exhibit a therapeutic benefit.

There is an enormous medical need for safe and effective therapeutics that treat neuropsychiatric and neurologic disorders and we believe genetic engineering provides the answer, said Dr. Azam, Empyreans Chief Executive Officer. By applying our genetic engineering platform to make precise modifications to the genomes of fungi and plants, we can change the amount and kind of neuroactive small molecules they produce, with the goal of developing safe and effective treatments for difficult-to-treat diseases of the CNS.

The companys developmental pipeline includes fungal alkaloids, cannabinoids, and other neuroactive compounds, such as N,N-Dimethyltryptamine (DMT), for the potential treatment of major depressive disorder (MDD), post-traumatic stress disorder (PTSD), neurologic disorders, substance abuse and dependence, and chronic pain. Investigational New Drug (IND) enabling studies of the companys first genetically engineered encapsulated mushroom drug product are currently underway, and the company aims to enter the clinic for MDD in 2023.

Fungal alkaloids and cannabinoids have shown promise in treating depression, PTSD, anxiety, and other neuropsychiatric and neurologic disorders, said Dr. Grossman, Empyreans Chief Medical Officer. We believe our approach of genetically engineering fungi and plants can improve their safety and efficacy and will ultimately help to address the substantial unmet medical need in patients who suffer from these diseases.

As part of its genetic engineering platform, the company has licensed CRISPR/Cas9 technology from ERS Genomics for genetic engineering applications related to its therapeutic pipeline.

Dr. Azam was previously President and Chief Executive Officer of Tmunity Therapeutics, a biotech developing genetically engineered cell therapies for applications in cancer. Before Tmunity, he was Global Head of Cell & Gene Therapies at Novartis, where he was responsible for commercial operations, business development licensing, new product commercialization, clinical development, regulatory affairs, and other aspects of the global cell and gene therapies business. He was Chief Executive Officer of Novaccel Therapeutics, Chief Medical Officer of Aspreva Pharmaceuticals, and earlier in his career, held positions at Johnson & Johnson, GSK, and Pfizer. Dr. Azam received his M.D. from the University of Liverpool School of Medicine and is board certified in obstetrics and gynecology in the United Kingdom.

Before joining Empyrean, Dr. Grossman was Chief Medical Officer of Mesoblast Ltd. and President and Chief Medical Officer of Glenmark Pharmaceuticals. He has held executive leadership positions in large pharmaceutical companies, including Eli Lilly, Johnson & Johnson, Bristol Myers Squibb, and Sunovion. He has been responsible for leading the development, approval, and supporting the launch of numerous global medications addressing significant unmet medical needs across therapeutic areas, particularly in the CNS. He has held academic appointments and has authored numerous scientific publications. He was trained in psychiatry at Hahnemann University in Philadelphia and at the National Institute of Mental Health in Bethesda, Maryland and completed a Fellowship in the Section on Clinical Pharmacology at the National Institutes of Health. Dr. Grossman is a board-certified psychiatrist and Fellow of the American Psychiatric Association.

About Empyrean Neuroscience

Empyrean Neuroscience is a genetic engineering company developing a pipeline of neuroactive therapeutics to treat a range of neuropsychiatric and neurologic disorders. Through precision genetic modification, transformation, and regeneration of fungi and plants, the platform allows for the creation of small molecule therapeutics. In addition, the platform enables the discovery of novel small molecules that may exhibit therapeutic properties. The company is based in New York City and Cambridge, UK.

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Empyrean Neuroscience Launches with $22M Series A and Genetic Engineering Platform to Advance Pipeline of Neuroactive Compounds Targeting CNS...

Neuroscience

A New Protein That May Contribute to Alzheimers Disease Identified – Neuroscience News

Summary: The GM2A protein reduces neural firing and induces a loss of neurite integrity.

Source: Brigham and Womens Hospital

Alzheimers disease (AD) currently has no cure and is predicted to affect over 100 million people worldwide by 2050.

Ongoing research is focused on two key neurotoxic proteins: amyloid beta (A) and tau. While these proteins have been shown to be associated with AD, for some people with the disease, the levels of A and tau do not consistently explain or correlate with the severity of cognitive decline.

To identify other proteins that may be directly involved with fundamental aspects of AD, like synaptic loss and neurodegeneration, investigators at Brigham and Womens Hospital, a founding member of the Mass General Brigham healthcare system, exposed laboratory neurons to human brain extracts from about 40 people who either had AD, were protected from AD despite having high A and tau levels, or were protected from AD with little or no A and tau in their brains.

The researchers identified and validated ganglioside GM2 activator (GM2A) as a protein able to reduce neuronal firing and induce a loss of neurite integrity. These protein characteristics may contribute to the cause of AD, progression of the disease, or both.

Our data helps identify a new and potentially important protein that may be associated with the pathogenesis of Alzheimers disease, said senior author Tracy Young-Pearse, PhD, from the Department of Neurology.

Interestingly, GM2A has been previously implicated as a causative agent in a lysosomal storage disorder very similar to Tay-Sachs disease, another condition like AD that destroys neurons.

Author: Haley BridgerSource: Brigham and Womens HospitalContact: Haley Bridger Brigham and Womens HospitalImage: The image is in the public domain

Original Research: Open access,Elevated ganglioside GM2 activator (GM2A) in human brain tissue reduces neurite integrity and spontaneous neuronal activity by Tracy Young-Pearse et al. Molecular Neurodegeneration

Abstract

Elevated ganglioside GM2 activator (GM2A) in human brain tissue reduces neurite integrity and spontaneous neuronal activity

Alzheimers Disease (AD) affects millions globally, but therapy development is lagging. New experimental systems that monitor neuronal functions in conditions approximating the AD brain may be beneficial for identifying new therapeutic strategies.

We expose cultured neurons to aqueous-soluble human brain extract from 43 individuals across a spectrum of AD pathology. Multi-electrode arrays (MEAs) and live-cell imaging were used to assess neuronal firing and neurite integrity (NI), respectively, following treatments of rat cortical neurons (MEA) and human iPSC-derived neurons (iN) with human brain extracts.

We observe associations between spontaneous activity and A42:40 levels, between neurite integrity and oligomeric A, and between neurite integrity and tau levels present in the brain extracts. However, these associations with A and tau do not fully account for the effects observed. Proteomic profiling of the brain extracts revealed additional candidates correlated with neuronal structure and activity. Neurotoxicity in MEA and NI assays was associated with proteins implicated in lysosomal storage disorders, while neuroprotection was associated with proteins of the WAVE regulatory complex controlling actin cytoskeleton dynamics. Elevated ganglioside GM2 activator (GM2A) associates with reductions in both NI and MEA activity, and cell-derived GM2A alone is sufficient to induce a loss of neurite integrity and a reduction in neuronal firing.

The techniques and data herein introduce a system for modeling neuronal vulnerability in response to factors in the human brain and provide insights into proteins potentially contributing to AD pathogenesis.

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A New Protein That May Contribute to Alzheimers Disease Identified - Neuroscience News

Neuroscience

NUCALM WILL UNLEASH THE POWER OF YOUR MENTAL STATE AT THE 2022 NEUROSCIENCE SUMMIT – PR Newswire

LOS ANGELES, Oct. 18, 2022 /PRNewswire/ -- NuCalm CEO Jim Poole will be this year's featured presenter at the 2022 Neuroscience Summit. The highly anticipated event will be broadcasting live, worldwide from October 20th to October 23rd, available on Roku TV and other streaming platforms. The brain health and wellness event features a stellar lineup of New York Times Bestselling authors, Harvard scientists and mental health experts. Complete details are on the event's website: http://www.nsciencesummit.com.

NuCalm research and their studies have led to a patented neuroscience technology unleashing the brain's unlimited potential. By participating in this year's summit, thousands of new users will have the chance see how they can take control of their lives and achieve their goals. NuCalm's unprecedented work in neuroscience gives individuals the power to improve memory, accelerate the learning process and most importantly the ability to harness calm. Calm, the absence of harmful emotions such as fear, nervousness, anxiety, panic or anger, can be leveraged to provide emotional intelligence to help leaders make the decisions necessary to achieve success.

NuCalm's CEO, Jim Poole, extols the impact that the 2022 Neuroscience Summit will have by saying, "This year's event will offer thousands of people a look into our neuroscience platform that changes the game for so many people. The abilities that NuCalm unlocks is the beginning of unleashing the full human potential." Poole said, "Through decades of research and development, we've made it possible to construct and consciously control the most complicated and powerful computing system, your brain. Drugs and stimulants are no longer necessary for one to leverage their brain wave frequencies to overcome obstacles and achieve their goals."

To date, millions of people across the globe have benefitted from regular use of NuCalm (www.NuCalm.com). This patented, clinically proven technology allows you to flip the switch from stress to rest and recovery within minutes, without drugs or side-effects. Since 2009, NuCalm has been used in over two million surgical procedures and used bysports teams, the military, the FBI, cancer patients, PTSD sufferers, pilots, busy executives and many others.

Contact for NuCalm:Alfred HoptonCapstone Communications Company[emailprotected]

Laurie D. MuslowIt's All Good Entertainment Inc.818-808-0868 Office Direct[emailprotected]

David PooleChief Business OfficerNuCalm617-259-0877[emailprotected]

For more info visit http://www.nucalm.comor call 800-810-1701 to speak to a representative.

SOURCE NuCalm

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NUCALM WILL UNLEASH THE POWER OF YOUR MENTAL STATE AT THE 2022 NEUROSCIENCE SUMMIT - PR Newswire

Neuroscience

Neuroscience Research Fellow Discovers the Power of Perseverance – St. Lawrence University Saints

Nadiana Acevedo 24 isnt afraid of a challenge. When she set out to investigate the effects of an anti-cancer drug this summer, she discovered that sometimes the best learning experiences can come from trial and error.

As part of the Collegiate Science and Technology Entry Program (CSTEP), Nadiana spent eight weeks conducting research alongside Professor of Biology and Psychology Ana Estevez. The scholar program is designed to increase the number of historically underrepresented and economically disadvantaged students in mathematics, science, technology, and health-related fields.

Nadiana shared what fueled her curiosity for research and how she defines success.

(Note: Responses have been edited for length.)

Major: Neuroscience

Hometown: Buffalo, New York

Project Title: "Observing Cell Viability of HT-22 Hippocampal Cells When Exposed to Anti-Cancer Dye MKT-077"

The focus of my research is looking at an anti-cancer dye, MKT-077. This dye is known to be selective to cancer cells meaning it only kills cancer cells. I am testing the drug on a mouse hippocampal neuronal cell line called HT-22 (brain cells) to observe the drug's effect on the cells' viability.

Cancer research is challenging and exciting because it is full of trial and error. I was interested in looking at how this drug would affect neuronal cells because there is a lack of data specific to neurons. I was intrigued that MKT-077 is selective to cancer cells because other drugs kill both healthy and cancerous cells.

The research process was difficult at times because my mentor and I did not know how the MKT-077 would affect the HT-22 cells. The data seemed off in the beginning. We weren't sure if there was an issue with fluorescence when the microplate reader was collecting data. We had to run a test to determine if the MKT-077 had its own fluorescence that would interfere with the dye we used to measure viability. The data showed no conflict between the MKT-077 and the CYQUANT dye we used to measure cell viability.

I did not get discouraged by the research outcomes and was able to complete my summer research and presented my findings.

Dr. Ana Estevez is an amazing advisor and mentor. I built a connection with her over the summer and learned many skills. She has helped me become a well-rounded researcher.

It is possible to succeed and gain knowledge regardless of the data outcome. There is always something to gain from every experience and there is always something new to discover.

Learn About Research

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Neuroscience Research Fellow Discovers the Power of Perseverance - St. Lawrence University Saints

Neuroscience

COVID-19 Linked to Excessive Destruction of Connections Between Nerve Cells – Neuroscience News

Summary: COVID-19 infection causes microglia to excessively engulf synaptic structures and the upregulation of factors involved in phagocytosis.

Source: Karolinska Institute

Researchers at Karolinska Institutet have in a new study used cellular reprogramming to create human three-dimensional brain models and infected these models with SARS-CoV-2.

In infected models, the brain immune cells excessively eliminated synapses and acquired a gene expression pattern mimicking what has been observed in neurodegenerative disorders.

The findings could help to identify new treatments against persistent cognitive symptoms after a COVID-19 infection.

Multiple studies have reported persistent cognitive symptoms after a COVID-19 infection but the underlying mechanisms for this remains unknown.

The researchers behind the study, published as an Immediate Communication in the journalMolecular Psychiatry, have from human induced pluripotent stem (iPS) cells created three-dimensional models of the brain in a dishso-called brain organoids.

The model differs from previous organoid models as the researchers also included the brainimmune cellsmicrogliain the model.

In the infected models, microglia excessively engulfed synaptic structures and displayed upregulation of factors involved in phagocytosis. The developed model and the findings in the study could help to guide future efforts to target cognitive symptoms in the aftermath of COVID-19 and other neuroinvasive viral infections.

Cognitive deficits after the infection

Interestingly, our results to a large extent mimic what has recently been observed in mouse models infected with other neuroinvasive RNA viruses such as the West Nile virus. These viruses are also linked to residual cognitive deficits after the infection, and a persisting activation of microglia leading to an excessive engulfment of synapses, which has been suggested to drive these symptoms.

Multiple studies have now also reported remaining cognitive symptoms after a COVID-19 infection, as well as an increased risk of receiving a diagnosis of a disorder characterized by cognitive symptoms, says co-first author of the study Samudyata, postdoctoral fellow in Sellgren lab at the Department of Physiology and Pharmacology at Karolinska Institutet.

Connections to Parkinsons and Alzheimers disease

Microglia are the resident immune cells of the brain but also carries out important regulatory functions of the neuronal circuitries in the developing and adultbrain. One of these crucial functions is to engulf unwanted synapses, a process that is believed to improve and maintain cognitive functions.

However, excessive engulfment of synapses has been linked to both neurodevelopmental disorders, such as schizophrenia, as well as to neurodegenerative disorders including Alzheimers disease.

By sequencing genes insingle cells, the authors could also study how different cell types in the model responded to the virus.

Microglia displayed a distinct gene signature largely characterized by an upregulation of interferon-responsive genes, and included pathways previously linked to neurodegenerative disorders such as Parkinsons and Alzheimers disease.

This signature was also observed at a later time-point when the virus load was minimal, says co-author of the study Susmita Malwade, doctoral student in Sellgren lab at the Department of Physiology and Pharmacology at Karolinska Institutet.

The researchers will now study how different pharmacological approaches can reverse the observed changes in the infected models.

Author: Press OfficeSource: Karolinska InstituteContact: Press Office Karolinska InstituteImage: The image is in the public domain

Original Research: Open access.SARS-CoV-2 promotes microglial synapse elimination in human brain organoids by Samudyata et al. Molecular Psychiatry

Abstract

SARS-CoV-2 promotes microglial synapse elimination in human brain organoids

Neuropsychiatric manifestations are common in both the acute and post-acute phase of SARS-CoV-2 infection, but the mechanisms of these effects are unknown.

In a newly established brain organoid model with innately developing microglia, we demonstrate that SARS-CoV-2 infection initiate neuronal cell death and cause a loss of post-synaptic termini.

Despite limited neurotropism and a decelerating viral replication, we observe a threefold increase in microglial engulfment of postsynaptic termini after SARS-CoV-2 exposure.

We define the microglial responses to SARS-CoV-2 infection by single cell transcriptomic profiling and observe an upregulation of interferon-responsive genes as well as genes promoting migration and synapse engulfment.

To a large extent, SARS-CoV-2 exposed microglia adopt a transcriptomic profile overlapping with neurodegenerative disorders that display an early synapse loss as well as an increased incident risk after a SARS-CoV-2 infection.

Our results reveal that brain organoids infected with SARS-CoV-2 display disruption in circuit integrity via microglia-mediated synapse elimination and identifies a potential novel mechanism contributing to cognitive impairments in patients recovering from COVID-19.

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COVID-19 Linked to Excessive Destruction of Connections Between Nerve Cells - Neuroscience News

Neuroscience

Can Obesity and Stress Influence Appetite? – Neuroscience News

Summary: Stress impacts the brains response to food, researchers report. Additionally, both lean and obese people react to food cues in brain areas associated with reward and cognitive control.

Source: Johns Hopkins Medicine

In a series of experiments using functional magnetic resonance imaging (fMRI) to measure brain activity across networks in the brain, Johns Hopkins Medicine researchers looked at how stress might increase appetite in obese and lean adults.

The researchers found that stress impacts the brains responses to food, and that both lean and obese adults react to food cues in areas of the brain associated with reward and cognitive control.

The findings of the studywere published Sept. 28 inPLOS ONE.

For the study, the researchers analyzed data from 29 adults (16 women and 13 men), 17 of whom had obesity and 12 of whom were lean. Participants completed two fMRI scans, one following a combined social and physiological stress test.

Participants were given afood word reactivity testduring both scans. Thistestinvolved looking at how peoples brains reacted to food words, such as menu items on a chalkboard.

To maximize the appetitive response in the brain, the researchers asked participants to imagine how each food looked, smelled and tasted, and how it would feel to eat it at that moment.

They were also asked how much they wanted each food, and if they felt they should not eat that food, to see how they approached decision-making related to each food.

The experiments showed that obese and lean adults differ somewhat in their brain responses, with obese adults showing less activation of cognitive control regions to food words, especially to high-calorie foods, like for example, grilled cheese, says lead researcherSusan Carnell, Ph.D., associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine.

The study also showed that stress impacts brain responses to food. For example, obese individuals showed greater activation of the orbitofrontal cortex, a brain reward region, after the stress test.

We also found evidence for links between the subjective stress experienced and brain responses in both groups. For example, lean individuals who reported higher stress following the test showed lower activation of the dorsolateral prefrontal cortex, a key brain area for cognitive control, says Carnell.

Author: Marisol MartinezSource: Johns Hopkins MedicineContact: Marisol Martinez Johns Hopkins MedicineImage: The image is in the public domain

Original Research: Open access.Obesity and acute stress modulate appetite and neural responses in food word reactivity task byCarnell et al. PLOS ONE

Abstract

Obesity and acute stress modulate appetite and neural responses in food word reactivity task

Obesity can result from excess intake in response to environmental food cues, and stress can drive greater intake and body weight. We used a novel fMRI task to explore how obesity and stress influenced appetitive responses to relatively minimal food cues (words representing food items, presented similarly to a chalkboard menu).

Twenty-nine adults (16F, 13M), 17 of whom had obesity and 12 of whom were lean, completed two fMRI scans, one following a combined social and physiological stressor and the other following a control task. A food word reactivity task assessed subjective food approach (wanting) as well as food avoidant (restraint) responses, along with neural responses, to words denoting high energy-density (ED) foods, low-ED foods, and non-foods.

A multi-item ad-libitum meal followed each scan. The obese and lean groups demonstrated differences as well as similarities in activation of appetitive and attention/self-regulation systems in response to food vs. non-food, and to high-ED vs. low-ED food words.

Patterns of activation were largely similar across stress and non-stress conditions, with some evidence for differences between conditions within both obese and lean groups. The obese group ate more than the lean group in both conditions.

Our results suggest that neural responses to minimal food cues in stressed and non-stressed states may contribute to excess consumption and adiposity.

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Can Obesity and Stress Influence Appetite? - Neuroscience News

Neuroscience

Reductionism as a Dead End in Neuroscience Captured in an Essay – Walter Bradley Center for Natural and Artificial Intelligence

University of Sussex professor of cognitive and computational neuroscience Anil K. Seth, during a routine dismissal of Ren Descartes (15961650), assures us, It looks like scientists and philosophers might have made consciousness far more mysterious than it needs to be.

More mysterious than it needs to be?

As noted earlier, what makes understanding the human mind necessarily complex is that it is both the entity we are trying to perceive and the tool by which we hope to perceive it. Such a problem is like trying to imagine a five-dimensional box in relation to the real world. Unlike the five-dimensional box, consciousness is part of the life experience of every human being.

How would Dr. Seth unravel the problem? In a classic essay, he reassures us,

Once, biochemists doubted that biological mechanisms could ever explain the property of being alive. Today, although our understanding remains incomplete, this initial sense of mystery has largely dissolved. Biologists have simply gotten on with the business of explaining the various properties of living systems in terms of underlying mechanisms: metabolism, homeostasis, reproduction and so on. An important lesson here is that life is not one thing rather, it has many potentially separable aspects.

Well, wait. We know a great deal more than we did centuries ago about the circumstances that enable a life form to keep itself alive and pass on that state to a further generation. But we are still at a complete loss as to the origin of life.

This is despite hundreds of speculative papers published every year. Eminent chemist James Tour has often remarked on well, expostulated about this problem. Its fascinating. It is especially relevant to the search for life on other planets in our galaxy. But looking for evidence of lifes existence is quite different from explaining lifes origin.

Origin of consciousness is in roughly the same state as origin of life. We have vast amounts of useful information about being conscious but we have no idea how it comes about.

What does Dr. Seth say about consciousness (or selfhood)?

Of the many distinctive experiences within our inner universes, one is very special. This is the experience of being you. Its tempting to take experiences of selfhood for granted, since they always seem to be present, and we usually feel a sense of continuity in our subjective existence (except, of course, when emerging from general anaesthesia). But just as consciousness is not just one thing, conscious selfhood is also best understood as a complex construction generated by the brain.

There is the bodily self, which is the experience of being a body and of having a particular body. There is the perspectival self, which is the experience of perceiving the world from a particular first-person point of view. The volitional self involves experiences of intention and of agency of urges to do this or that, and of being the causes of things that happen. At higher levels, we encounter narrative and social selves. The narrative self is where the I comes in, as the experience of being a continuous and distinctive person over time, built from a rich set of autobiographical memories. And the social self is that aspect of self-experience that is refracted through the perceived minds of others, shaped by our unique social milieu.

In daily life, it can be hard to differentiate these dimensions of selfhood.

The problem isnt so much that it is hard to differentiate these dimensions of selfhood as that it is hard to believe that a simple, reductionist approach to the question will provide much insight.

For example, Dr. Seth writes, The specific experience of being you (or me) is nothing more than the brains best guess of the causes of self-related sensory signals. That seems inconsistent with the council of selves that Dr. Seth himself sketches out in the paragraph quoted above. If he is right, your local town council votes may be less frenetic at any given time than what is going on in your own mind but that is not an argument for reductionism.

It becomes even more confusing when Dr. Seth tells us,

This returns us one last time to Descartes. In dissociating mind from body, he argued that non-human animals were nothing more than beast machines without any inner universe. In his view, basic processes of physiological regulation had little or nothing to do with mind or consciousness. Ive come to think the opposite. It now seems to me that fundamental aspects of our experiences of conscious selfhood might depend on control-oriented predictive perception of our messy physiology, of our animal blood and guts. We are conscious selves because we too are beast machines self-sustaining flesh-bags that care about their own persistence.

So, contemplating the vast mystery as well as complexity of consciousness, Dr. Seth asserts that it shows that we too are beast machines.

Actually, it provides a convincing demonstration of how reductionism does not work well in neuroscience. At most, it would mean that animal consciousness is more complex than we have earlier supposed. For that, at least, we have a growing body of evidence.

You may also wish to read: Psychiatry has always been difficult but its unclear how trashing almost every philosophical tradition from which it is approached will really help. Understanding the human mind is necessarily complex because it is both what we are trying to perceive and the tool by which we hope to perceive it.

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Reductionism as a Dead End in Neuroscience Captured in an Essay - Walter Bradley Center for Natural and Artificial Intelligence

Neuroscience

Patients With Clinical Depression Stopped Seeking Treatment During the COVID Waves – Neuroscience News

Summary: During the COVID-19 pandemic, the number of patients admitted to hospitals for clinical depression care dropped significantly. However, the number of people seeking outpatient care for depression increased.

Source: European College of Neuropsychopharmacology

In the first study of its kind, German researchers have shown that the COVID pandemic saw a huge drop in the number of patients being admitted to hospital for clinical depression.

Independently of these national statistics, the researchers found that the number of outpatients they dealt with increased over the same period in their department. As inpatient treatment offers more intensive levels of care, this implies that many patients did not receive care appropriate to their condition.

It is not yet known if this shift in treatment is also seen in other countries.

The researchers, from the University Hospital in Frankfurt, looked at German national databases. They found that during the first COVID wave new hospitalisations for first time clinical depression dropped by 57.5%, from 13457 in January 2020 down to 5723 in April 2020. In the same period, the number of patients being hospitalised for recurrent depression dropped by 56.3%, from 22188 down to 9698.

Lead researcher, Dr Mareike Aichholzer said We also saw a decrease in inpatient treatment of recurrent depression in our own hospital in Frankfurt. In addition to the stricter admission rules, this rather seemed to be due to a drop in demand from the patients themselves.

In contrast, the number of new outpatients being treated for clinical depression at the University Hospital in Frankfurt remained stable and the number of patients with recurrent depression showed a significant increase between 2019 and 2021.

However, Dr Aichholzer notesThis is data from a single center, so we need to wait to see what other centers say.

She continued, The results indicate that patients who have repeatedly suffered from depression during their lives were less likely to be admitted to hospital during the pandemic. However, these patients are often so severely affected by depression that outpatient treatment alone is not sufficient to bring about a satisfactory improvement in symptoms.

The result is that patients lose their quality of life in the long term. The actual reason for this observation is unclear. Although our study was not designed to identify the reasons for those changes, we however suspect that clinically depressed patients in particular withdraw more often from society/their friends/their family and that this behavior was more common during the times of the lock-down and the strict hygiene guidelines.

Moreover, we suspect, that clinically depressed patients avoided the hospital, because they were afraid of being infected with COVID-19 on the ward.

The data from our hospital in Frankfurt indicates that patients with clinical depression seem to have withdrawn themselves, rather than seeking adequate mental health help. To be prepared for the winter with potentially increasing COVID numbers, we have to provide easily accessible help and raise awareness for this topic.

Clinical depression, also known as Major Depressive Disorder (MDD) is a serious mental illness, affecting more than 6% of Europeans at any one time. The majority of sufferers can be treated with pharmaceuticals and/or counseling, although a minority of patients dont respond to treatment.

Commenting, Professor Brenda Penninx, Professor of psychiatric epidemiology at the Department of Psychiatry, University Medical Centre, Amsterdam, said:

The figures found by the Frankfurt team confirm a familiar pattern. We have recently found that quite a few countries are beginning to report a decreased pattern of mental health care use during the first pandemic years.

It is extremely important that in the next few years we follow whether postponed treatments may result in increased mental health problems.

This also illustrates that mental health care deserves adequate clinical attention during future pandemics.

This is an independent comment, Professor Penninx was not involved in this research.

Author: Tom ParkhillSource: European College of NeuropsychopharmacologyContact: Tom Parkhill European College of NeuropsychopharmacologyImage: The image is in the public domain

Original Research: The findings will be presented at the 35thEuropean College of Neuropsychopharmacology

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Patients With Clinical Depression Stopped Seeking Treatment During the COVID Waves - Neuroscience News

Neuroscience

How I used my background in neuroscience to make it as a lawyer – Legal Cheek

Bristows Gregory Bacon on his transition from academia to IP and what STEM students can offer law firms

Gregory Bacon, partner and patent litigation specialist at Bristows, is well-placed to discuss a career change from science to law. He completed a PhD in neuroscience at Oxford University and spent time as postdoctoral researcher at Kings College London.

Intellectual property is often considered one of the areas of law most accessible to those with a background in science, technology, engineering and mathematics (STEM). The highly technical nature of projects in this area offers an array of challenges for those with puzzle-oriented minds.

Bristows represents huge clients at the cutting-edge of the science and technology sector, working with mega-brands like Google, Facebook and Samsung. They also have an impressive life sciences client base and the firm worked with AstraZeneca and Oxford University on their Covid jab during the pandemic. Bringing new products and technologies to the commercial market can be a difficult process and Bacon specialises in helping clients navigate disputes over their patents.

He describes a case he is currently working on for a drug developed and licensed to treat multiple sclerosis, a lifelong condition affecting the brain and spinal cord. Treatments available still dont cure the disease, but they can significantly reduce underlying autoimmune reactions and slow disease progression, he explains. My client, a pharmaceutical company, developed and sells one of these treatments. Earlier this year, we made some new case law in relation to patent rights in the UK for that product, and whether these can be asserted before the patent is granted. Being an effective lawyer means coming up with solutions for your client, including sometimes ones that have not been tried before. Another case Bacon is working on involves a dispute between two pharmaceutical companies as to whether contractual royalties are payable in relation to a product that is licensed and sold by one of them for the treatment of rare forms of childhood epilepsy.

Whilst a STEM background is not a requirement to be a good patent lawyer, Bacon continues, it helps to have a basic grounding of scientific knowledge. He is quick to point out that the niche knowledge from his PhD is often not as helpful as the ability to interpret evidence. Being able to take data and understand it is key. For example, you need to be able to read scientific literature and understand how the information in that article can support your case or maybe actually supports the other sides case! Bacon says.

Enthusiasm for learning about technology is also an important quality for this kind of work, which is often something that STEM students develop through their studies. He says:

You need to want to keep learning about the technology as well as about the law. So when you get a new project on a chemical youve never heard of before or an interaction with an organ that youve never dealt with before, you think this sounds really interesting I want to get to know more!

Bacon acknowledges that his transition from science into law is made more unusual by his direct route. Strangely, I didnt go for a vacation scheme, I went straight for a training contract. I was offered an interview here at Bristows 20 years ago, and the interview went well. After accepting their offer of a job and completing his conversion course, Bacon started his training contract with the firm. I just loved every aspect of it, every seat! he reveals. But his interest in patent law had already taken root and after qualifying, he was offered a permanent position in their patents team.

After twenty years with Bristows, Bacons enthusiasm for what he does has in no way diminished. He describes finding an unexpected source of enjoyment in the management responsibilities that come with being a partner. It is quite an unusual step to go from not having any management responsibilities to having almost the full suite of management responsibilities, he explains. It brings with it a whole host of extra skills that you have to have to develop to be a partner. After eight or ten years of your post-qualification career, you take on all these new responsibilities: training junior colleagues, recruitment, winning client pitches and keeping clients happy. I think I enjoy this almost as much as doing the fee-earning work for the clients.

This split between his responsibilities as a fee earner and as a partner is also something that characterises his daily work. My day is split around 70:30. Seventy percent of my time is spent doing legal work, calls with clients, deciding on strategy, drafting documents, preparing cases for court, reading technical documents and speaking with international lawyers. Then the remainder of my time is involved in the management of the group, my department, and the wider firm. This includes ensuring my junior colleagues have enough work and theyre getting enough exposure to the right levels of work. And some general admin of course!

Considering his own career journey, what advice would he give to students looking at making the transition from STEM to law?

Do your research, Bacon stresses. Try and go to an open day or a law fair. If you can really get to see the firm as it operates behind the scenes, youll get a better feel for what the job looks like. Thats important because if youre a STEM student, youre looking at around a four-year process before youre qualified as a solicitor, and youve got something to show for all that work. So do the research and make sure it is something you want to invest four years of your time into.

Gregory Bacon will be speaking at STEM Focus: Life as an intellectual property lawyer with Bristows, a virtual student event taking place on Thursday 20 October. You can apply to attend the event, which is free, now.

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Neuroscience

Research Paves Way for Innovative Theory of Cognitive Processing – Neuroscience News

Summary: A new theory suggests glial cells, specifically astrocytes, play a key role in cognitive processing.

Source: University Health Network

A team of scientists from the Krembil Brain Institute, part of the University Health Network in Toronto, and Duke University in Durham, North Carolina, has developed the first computer model predicting the role of cortical glial cells in cognition.

The paper was published today in the prestigious journalProceedings of the National Academy of Sciences(PNAS).

The role of neurons is well documented, but neurons are interspersed with glial cells and many synapses in the brain have glia nearby, says Dr. Maurizio De Pitt, a scientist at the Krembil Brain Institute and the first author of the study. We currently do not understand how neurons and glia work together, or how glial dysfunction contributes to cognitive deficits.

Glial cells are abundant throughout the brain and play several important roles. These cells have long been thought to be passive bystandersphysically supporting neurons and synapses, bringing nutrients to neurons, and removing toxins and waste products. However, scientists have recently discovered that glia interact with neurons in a fashion similar to the way that neurons communicate with one another through chemical signals.

This paper presents the first theory of the role glia play in cognitive processing, in the brain. The type of glial cells that we studyknown as astrocytescan modify the activity of our brain circuits and influence the way we behave, says Dr. De Pitt.

The study looked at the role of astrocytes in working memory, which is the ability to store information for ongoing tasks, such as following the storyline of a movie or counting to ten.

We know that astrocytes release specialized chemical signals and we have shown that this signalling could mediate different readouts of working memory, says Dr. De Pitt.

Revealing that chemical interactions between neurons and astrocytes could be at the core of working memory, also tells us what could go wrong when we have working memory deficits, which are often warning signs of major brain disorders.

He adds, If we want to truly understand dysfunction in working memory, we need to consider the interaction between glial cells and neurons.

Also noted in the article:

Like radio systems, synapses have been traditionally thought to transmit on a single frequency band. Taking astrocytes into account, we now know there can be multiple frequency bands.

It is generally believed that different forms of working memory rely on a variety of circuits; however, this study shows that the same neuron-glial circuits could encode for various forms of working memory.

The way that astrocytes are arranged with respect to neurons could control our working memory capacity, or how many things we can keep in mind simultaneously.

Currently, there are no effective techniques to record glial activity in the human brain. The researchers hope to eventually create a high-fidelity modela digital twinof the brains neuron-glia circuits, from genes to cells.

Such a model can help to uncover markers of neuron-glial interactions and improve the diagnosis and treatment of various brain diseases, such as Alzheimers, Parkinsons and epilepsy.

With our new theory, we are not just looking at the brain in black and whitethat is, whether given neuron populations are active or inactive. Rather, we are viewing the brain in technicolour, gaining a deeper understanding of cellular communication by including glia and their signalling, says Dr. De Pitt.

This gives us a much more comprehensive and realistic picture of the complexity of the brain.

As technology advances, De Pitt and his team at the Krembil will use their models to develop techniques to modify neuron-glial circuit activity to treat disease. Our ultimate goal is to study neuron-glial interactions to uncover new therapeutic targets for brain disorders.

Funding: This work was funded by an FP7 Marie Skodowska-Curie International Outgoing Fellowship.Research at Dr. De Pitts lab is supported by operating grants from the Krembil Research Institute, the European Research Commission, the Krembil Foundation and UHN Foundation.

Author: Ana FernandesSource: University Health NetworkContact: Ana Fernandes University Health NetworkImage: The image is in the public domain

Original Research: Closed access.Multiple forms of working memory emerge from synapseastrocyte interactions in a neuronglia network model by Maurizio De Pitt et al. PNAS

Abstract

Multiple forms of working memory emerge from synapseastrocyte interactions in a neuronglia network model

Persistent activity in populations of neurons, time-varying activity across a neural population, or activity-silent mechanisms carried out by hidden internal states of the neural population have been proposed as different mechanisms of working memory (WM).

Whether these mechanisms could be mutually exclusive or occur in the same neuronal circuit remains, however, elusive, and so do their biophysical underpinnings.

While WM is traditionally regarded to depend purely on neuronal mechanisms, cortical networks also include astrocytes that can modulate neural activity.

We propose and investigate a network model that includes both neurons and glia and show that gliasynapse interactions can lead to multiple stable states of synaptic transmission.

Depending on parameters, these interactions can lead in turn to distinct patterns of network activity that can serve as substrates for WM.

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Research Paves Way for Innovative Theory of Cognitive Processing - Neuroscience News